Amiodarone HCl

Catalog No.S1979

Amiodarone HCl Chemical Structure

Molecular Weight(MW): 681.77

Amiodarone HCl is a sodium/potassium-ATPase inhibitor and an autophagy activator, used to treat various types of cardiac dysrhythmias.

Size Price Stock Quantity  
In DMSO USD 130 In stock
USD 97 In stock
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1 Customer Review

  • Drugs across therapeutic indications induce lipid formation in hiPS-CM. Lipid accumulation was detected in cardiac cells using the LipidTox plate-based fluorescent assay on the Thermo Scientific CellInsight High Content platform. A) Ten drugs increased lipid levels in hiPS-CM following 48 h treatment. The lowest drug dose that induced a N1.5-fold increase in lipid formation is shown. B) Representative images (20×) from the assay are shown to the right. All drugs had >55% cell viability at 48 h at these tested concentrations. C) Of these 10 drugs, 8 significantly increased lipid accumulation following only 24 h treatment (images not shown). All drugs had >80% cell viability at 24 h at these drug doses. The graphs represent the mean fold-change of the lowest concentration of drug that significantly induced lipid formation >1.5-fold more than vehicle control. *P<0.05, **P<0.01, and ***P<0.0001.

    Toxicol Appl Pharmacol, 2015, 285(1):51-60.. Amiodarone HCl purchased from Selleck.

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Biological Activity

Description Amiodarone HCl is a sodium/potassium-ATPase inhibitor and an autophagy activator, used to treat various types of cardiac dysrhythmias.
Targets
Potassium channel [1]
In vitro

Amiodarone possesses an inhibitory effect on the fast sodium channel as well as on the slow calcium channel. Amiodarone also has non-competitive antisympathetic effects, and modulates thyroid function and phospholipid metabolism. Amiodarone penetrates deeply into the lipid matrix of the membrane, and is released from cardiac tissues very slowly when washed out. Amiodarone (44–88 μM) depresses Vmax of guinea pig papillary muscle without affecting the resting membrane potential, and that this Vmax inhibition is enhanced in a frequency- or use-dependent manner like Class I antiarrhythmic drugs. Amiodarone (50–88 μM) is also found to suppress the depolarization-induced spontaneous action potentials (abnormal automaticity) in ventricular muscles and in Purkinje fibers. [1]

In vivo Amiodarone (1.25–25 mg/kg) results in a decrease in sinus rate, a prolongation of effective and functional refractory periods of the atrioventricular node, and a frequency-dependent conduction delay in the atrioventricular node and in the ventricle of anesthetized dogs. Amiodarone (50 mg/kg/day, i.p. for 3–4 weeks) results in significant decreases in the current density of iK and ito in ventricular cells without affecting iCa and iK1 densities in rabbit. Amiodarone (AM) inhibits intracellular conversion from thyroxine (T4) to triiodothyronine (T3) via 5′-deiodination (5′DI) without affecting intracellular conversion from T4 to reverse T3 (rT3). [1]

Protocol

Solubility (25°C)

In vitro DMSO 23 mg/mL (33.73 mM)
Ethanol 11 mg/mL (16.13 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
3mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 681.77
Formula

C25H29I2NO3.HCl

CAS No. 19774-82-4
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03153072 Withdrawn Supraventricular Tachycardia Centre Hospitalier Universitaire Amiens September 6 2016 Phase 2
NCT03029169 Recruiting Supraventricular Arrhythmia|Septic Shock Charles University Czech Republic October 23 2017 Phase 4
NCT02668432 Enrolling by invitation New Onset Atrial Fibrillation|Severe Sepsis|Septic Shock The University of Texas Health Science Center at San Antonio May 2016 Phase 4
NCT02750319 Recruiting Thoracic Surgery|Atrial Fibrillation in High Risk Patients Memorial Sloan Kettering Cancer Center|Washington University School of Medicine|The Cleveland Clinic|Vanderbilt University School of Medicine April 2016 Phase 3
NCT02715687 Not yet recruiting Atrial Fibrillation Rambam Health Care Campus March 2016 Phase 3
NCT02341105 Recruiting Atrial Fibrillation Guy Amit|Population Health Research Institute January 2016 Phase 4

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID